To see how the serendipity wands are waved by evolutionary theorists, let’s look at the story of how certain Arctic codfish supposedly acquired the ability to produce an antifreeze protein in their blood – quite handy for a fish living in such a cold environment.
Researchers looked at seven related species of codfish.1 Three of them had a working antifreeze gene. A fourth had the core of the gene, but it was mutated so it wasn’t functional. The other three didn’t have the gene, but they did have sets of related 27 to 30 nucleotide sequences that seemed to be duplicates.
One of these three species also had what the researchers considered to be the ancestor of the antifreeze gene, a tiny sequence of just 9 nucleotides, coding for three amino acids – threonine, alanine, alanine – that could have formed the basis of the antifreeze protein in the other species.
By comparing similar areas of the genome in the related species, the researchers constructed what they considered to be the evolutionary story of the antifreeze protein. According to the story, a 27 to 30 nucleotide sequence was somehow prone to duplication, and this is precisely what it did. It duplicated to become four copies next to each other.
Out of the midst of this came the threonine-alanine-alanine sequence, the core of the antifreeze property. This was also duplicated multiple times, so the evolving gene would have just the right chemical properties to prevent ice crystals from growing in the blood of the codfish. This was how the functional part supposedly evolved.
However, the emerging gene wasn’t yet in a form that could be turned into a protein by the cell. For this, the gene would need a control sequence allowing it to be transcribed by ribosomes, and therefore manufactured. The control sequence somehow translocated its way over to the emerging gene, or the gene wandered over to a location where the control sequence was.
There also happened to be a sequence, one nucleotide away from the emerging gene, that could tag it for export from the cell and into the blood, exactly where it would need to go. According to the researchers, this export sequence didn’t originate anywhere else in the genome. It just happened to be in virtually the right place at the right time. The nucleotide separating the export sequence from the gene was deleted, and the end result was a fully functioning antifreeze gene, ideal for the formerly freezing codfish.
Now, this was a fairly impressive piece of research, and certain people viewed it as a fish-slap in the face to the idea that intelligence was required to produce a protein.2 However, there are three major problems with this codfish story, which should cause us to question whether it is even possible.
The first is the assumption that the lineage of species is correct and accurately reflects evolution moving toward the antifreeze gene. It assumes that the codfish species with the 9 nucleotide sequence was the source of the gene.
However, there are several clues that the real story might actually be the other way round. In one of the seven species they looked at, the antifreeze gene was almost intact, but contained mutations that inactivated it, likely because this species inhabited warmer water where antifreeze wasn’t needed. Losing the function posed no threat to the survival of this species, so natural selection wouldn’t need to preserve the gene. More likely then, in this species the sequence had become a pseudogene. It was losing information, devolving away from the antifreeze gene rather than evolving towards it.
If the order is wrong, it would explain why the so-called ancestor sequence, the threonine-alanine-alanine sequence of amino acids that forms the core of the antifreeze property, is present in one of the species without the antifreeze gene, along with the 27 to 30 letter sequences. In this scenario, it wouldn’t be an ancestor but simply a remnant, with much of the original gene mutated away. According to the researchers, the 27 to 30 nucleotide sequences contained substantial variations, suggesting significant mutations, which would also be consistent with the idea that they are remnants of the antifreeze gene that had been mutated.
It would also elegantly explain why a sequence tagging a protein for export from the cell into the blood just happened to be in virtually the right place. It may simply be a remnant of the original antifreeze gene, still in the same place it had been in all along!
The news reports related to the research give us another clue as to what might be the real story. It turns out, the codfish on the opposite side of the world, in the Antarctic, also have this antifreeze ability, although they supposedly evolved it in a different way.
For evolutionary theorists, this is an example of what they call “convergent evolution,” where the same function or feature is said to have evolved independently. However, perhaps it’s evidence that both Arctic and Antarctic codfish had this antifreeze ability, but some Arctic ones lost it. Indeed, since evolutionary theory contains the idea of common descent, isn’t it at least plausible that the assumed lineage is somehow incorrect, and that a common ancestor of both Arctic and Antarctic codfish had the antifreeze gene, but some species later lost it?
The second problem with the story is the extensive use of serendipity wands. The “duplication” wand is waved repeatedly, first so that multiple copies of the 27 nucleotide sequence are produced, and then again to make several perfect copies of the 9 nucleotide antifreeze sequence. In evolutionary storytelling, it doesn’t matter how likely or unlikely this is, compared with the other things that could have happened. As long as it’s not impossible, it is simply assumed to have happened.
Then the “translocation” wand is waved at least twice; once to get a control sequence from elsewhere, or to move the emerging gene to the control sequence; and once more to get rid of the single nucleotide that separated the potentially functional part of the gene from the sequence that would export the protein into the blood – which by a stroke of yet more incredible serendipity, just happened to be in virtually the right place.
To give a comparison, the almost functional gene found the equivalent of a parcel on its doorstep, containing just the right mechanism to get the protein into the blood. Don’t worry about probabilities. If it’s not impossible, it must have happened. Three species of Arctic codfish now have their antifreeze protein because the mechanism to get it into the blood just happened to be there.
The “magical steps” wand isn’t used in the codfish story. The researchers say this all happened in a non-coding region of DNA – that is, a region that doesn’t code for proteins – so the emerging gene didn’t code for a functional protein until all the parts came together. But if the gene didn’t have a function while it was going through its “duplication” and “translocation” phases, it wouldn’t be subject to natural selection. The implication is that these things must have evolved very fast, otherwise the emerging gene would be destroyed by mutations.
The third problem with the story is that the origins of the export and control sequences are vague. Where did they come from? Although the researchers suggest the emerging antifreeze gene might have somehow translocated over to a control sequence, they also provide evidence that both the control and expert sequences didn’t come from any existing protein-coding genes in the codfish genome, but originated de novo, which is a term used by biologists, meaning “of new.” In other words, the emerging gene might have found its way to a control sequence that wasn’t even there before! 3
The bottom line is this: according to the evolutionary story told by these researchers, the antifreeze protein came about as a result of a series of seemingly improbable, serendipitous events. But this raises a vital question, highly relevant to our discussion of what evolution can actually do.
1 Zhuang et al, “Molecular mechanism and history of non-sense to sense evolution of antifreeze glycoprotein gene in northern gadids”, PNAS, 2019. See also the article “Study of Arctic fishes reveals the birth of a gene – from ‘junk’” published on the Illinois News Bureau by Diana Yates, February 11, 2019. 2 See the post “The evolution of ‘irreducibly complex’ antifreeze proteins in a polar fish (and a fish-slap at Behe)” at Jerry Coyne’s blog whyevolutionistrue.com posted March 14, 2019. 3 See the section “Nongenic Origin of SP and Promoter Region” in the Zhuang et al paper. The export sequence is called a “signal peptide” (or “SP” for short), and the control sequence is called the “promoter.”